Anti-Kv11.1 (erg1)


Product#:APC-016

Sizes:
50 ml
0.2 ml


The KV11.1 (HERG) channel is a member of the ether-a-go-go (EAG) subfamily of voltage-dependent K+ channels that includes the related proteins KV11.2 and KV11.3 (erg2 and erg3). KV11.1 possess the signature structure of the voltage-dependent K+ channels: six membrane-spanning domains and intracellular N and C termini.

The KV11.1 current is characterized by strong inward rectification with slow activation and very rapid inactivation kinetics. The channel is expressed in the brain and heart (where it underlies the IKr current) and has a central role in mediating repolarization of action potentials.

Mutations in the KV11.1 channel cause inherited long QT syndrome (LQTS) or abnormalities in the repolarization of the heart that are associated with life-threatening arrhythmias and sudden death. All the identified KV11.1 mutations produce loss of function of the channel via several cellular mechanisms ranging from alterations of gating properties, alterations of channel permeability/selectivity and alterations in intracellular channel trafficking that decreases the number of channels that reach the cell membrane.1,2 Lately drug-induced forms of LQTS have been reported for a wide range of non-cardiac drugs including antihistamines, psychoactive agents and antimicrobials. All these drugs potently block the KV11.1 channel as an unintended side effect, prompting regulatory drug agencies to issue recommendations for the testing of new drugs for their potential KV11.1 blocking effect.

In addition, KV11.1 expression was found to be upregulated in several tumor cell lines of different histogenesis suggesting that it confers the cells some advantage in cell proliferation. Indeed, in several studies it has been shown that inhibition of the KV11.1 current leads to a decrease in tumor cell proliferation.3

Several venomous toxins from Scorpions are potent blockers (affecting the channels in the nanomolar range) of KV11.1channels. Among these the most potent and selective are Ergtoxin-1 (#RTE-450, 16nM)4 and BeKM-1 (#RTB-470, 3nM).5 In addition, the methanesulfonanilide class III antiarrhythmic agent E-4031, also blockes KV11.1 channel in the nanomolar range (#E-500, 7.7nM).6



Host:
Rabbit.
Epitope:

Peptide (CY)EEL PAGAP ELPQD GPT, corresponding to residues 1122-1137 of rat Kv11.1 (erg1) (Accession O08962).

Putative epitope location:

Intracellular, C-terminal part.

Homology:

Mouse - identical; human, dog, rabbit - 14/16 residues identical.

Reactivity Confirmed:
Rat, human.
Applications:
Western Blotting:
 
Western blotting of the lysate of HEK 293 cells, stably expressing HERG channels (1,2)
1. Anti-Kv11.1 (erg1) antibody (1:200).
2. Anti-Kv11.1 (erg1) antibody, preincubated with the control antigen.
Immunohistochemistry:
Mouse heart sections.
Immunoprecipitation:
 

Immunoprecipitation of the lysate of HEK 293 cells, stably expressing HERG with Anti-Kv11.1 (erg) antibody (#APC-016):

  1. Cell lysate.
  2. Cell lysate + protein A beads + Anti- Kv11.1(erg1) (#APC-016)
  3. Cell lysate + protein A beads + pre-immune rabbit serum.

 Red arrow indicates the Kv11.1 protein while the black arrow shows the IgG heavy chain.

Immunoblot was performed with the Anti- Kv11.1 (erg) extracellular (#APC-016)


References:
1. Curran, M.E. et al. (1995) Cell 80, 795.
2. Sanguinetti, M.C. et al. (1995) Cell 81, 299.
3. Pardo, L.A. et al. (2004) Physiology 19, 285.
4. Gurrola, G.B. et al. (1999) FASEB. J. 13, 953. 
5. Korolkova, Y.V. et al. (2001) J. Biol. Chem. 276, 9868.
6. Zhou, Z. et al. (1998) Biophys.J. 74, 230.
For research purposes only, not for human use.